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1.
Chinese Journal of Cardiology ; (12): 916-921, 2013.
Article Dans Chinois | WPRIM | ID: wpr-261458

Résumé

<p><b>OBJECTIVE</b>To investigate the association between the KCNE1 gene G38S and the KCNE4 gene E145D and atrial fibrillation in Uygur and Han populations living in Xinjiang.</p><p><b>METHODS</b>KCNE1 gene G38S and the KCNE4 gene E145D genotype and frequency were determined using PCR restriction fragment length polymorphism (PCR-RFLP) in 488 atrial fibrillation patients (237 Uygur and 251 Han residents) and 488 age-and-gender matched controls (237 Uygur and 251 Han residents).</p><p><b>RESULTS</b>Genotype and allele frequency of KCNE1 gene G38S were similar between atrial fibrillation group and control group in the Han population (P = 0.556, P = 0.946). In the Uygur population, there was a statistical difference between atrial fibrillation group and control group (P = 0.018, P = 0.003). Logistic regression analysis revealed the KCNE1 38 G was one of the independent risk factors for atrial fibrillation in the Uygur population (OR = 1.634, 95%CI: 1.192-2.240, P = 0.002). The KCNE4 gene E145D, genotype and allele frequency were significantly different between atrial fibrillation group and control group in the Uygur population and Han population (P = 0.041, P = 0.015;P = 0.032, P = 0.013) . Logistic regression analysis revealed the KCNE4 145D was one of the independent risk factors for atrial fibrillation in the Uygur population and Han population (OR = 1.636, 95%CI:1.173-2.281, P = 0.004; OR = 1.491, 95%CI:1.076-2.065, P = 0.016) .</p><p><b>CONCLUSIONS</b>KCNE1 G38S is not associated with atrial fibrillation in the Han population while the KCNE1 G38S is associated with atrial fibrillation in the Uygur population. KCNE4 gene E145D is associated with atrial fibrillation in both Uygur population and Han population.</p>


Sujets)
Sujet âgé , Femelle , Humains , Mâle , Adulte d'âge moyen , Asiatiques , Génétique , Fibrillation auriculaire , Ethnologie , Génétique , Études cas-témoins , Chine , Fréquence d'allèle , Génotype , Polymorphisme de nucléotide simple , Canaux potassiques voltage-dépendants , Génétique , Facteurs de risque
2.
Chinese Medical Journal ; (24): 1458-1463, 2013.
Article Dans Anglais | WPRIM | ID: wpr-350488

Résumé

<p><b>BACKGROUND</b>Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation (AF) was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF.</p><p><b>METHODS</b>Three groups of dogs were studied: adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL.</p><p><b>RESULTS</b>Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency.</p><p><b>CONCLUSION</b>These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AF.</p>


Sujets)
Animaux , Chiens , Facteurs âges , Apoptose , Fibrillation auriculaire , Remodelage auriculaire , Facteur de croissance du tissu conjonctif , Physiologie , Électrocardiographie , Fibrose , Méthode TUNEL , microARN , Physiologie , Myocarde , Anatomopathologie
3.
Chinese Journal of Medical Genetics ; (6): 455-458, 2008.
Article Dans Chinois | WPRIM | ID: wpr-308040

Résumé

<p><b>OBJECTIVE</b>To investigate the relationship between the low density lipoprotein receptor-related protein gene (LRP) 766C/T polymorphisms and Alzheimer's disease (AD) in Xinjiang Uygurs and Hans populations.</p><p><b>METHODS</b>Those included in the study were > or = 50 years of age and of either Xinjiang Uygur or Han descents. Two hundred and nine individuals had AD and 220 were healthy controls. They were recruited according to ADRDA-NINCDS criteriaîThe polymorphisms of the LRP gene were determined by the PCR-restriction fragment length polymorphism technique. The case-control analysis was adopted to analyze the frequencies of genotypes and alleles.</p><p><b>RESULTS</b>(1) The distribution of genotypes or alleles of LRP gene had significant differences between the AD group and the control group in both the Xinjiang Uygurs and Hans populations (P < 0.05). (2) The frequencies of genotypes and alleles were significantly different between the Han AD and Han control group (P < 0.05). (3) The frequencies of genotypes and alleles in those > or = 65 years were significantly different from that in others (P < 0.05). There was a significant increase of AD in the C allele carriers (OR=1.98, P < 0.05). (4) The frequencies of the CC genotype and C allele in female AD patients were higher than that in female controls (P < 0.05), and the C allele carriers had significant increase of AD (OR=2.927, P < 0.05).</p><p><b>CONCLUSION</b>The LRP 766C/T polymorphisms were significantly different between the Chinese Xinjiang Uygur and Han populations. The LRP 766C/T polymorphisms might be associated with AD in the Han population, in females and those of > or = 65 years old.</p>


Sujets)
Femelle , Humains , Mâle , Adulte d'âge moyen , Allèles , Maladie d'Alzheimer , Génétique , Asiatiques , Ethnologie , Génétique , Ethnies , Génétique , Génotype , Protéine-1 apparentée au récepteur des LDL , Génétique , Polymorphisme génétique
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